[Metabolic effects of barbiturates on the anoxic brain:free radical trapping]

Different mechanisms have been proposed to explain the protector effect of barbiturates in cerebral ischemia. Among these is the particularly attractive hypothesis that the protection is obtained by an inhibition of the oxydo-reduction process in the respiratory chain in the mitochondria upstream of the Q coenzyme. Keeping this enzyme in the quinone state prevents the formation of the three radical at the level of lipoid complexes of the cellular and sub-cellular membranes, thus assuring the upkeep of the integrity of these structures. The absence of the free radicals equally protects the morphology of the endothelium, in limiting the aggregation of platelets in the arterial vessel lumens. The existence of the three radicals in the organism and their noxious effects are well established, however, that the protection brought about by the barbiturates be the results of free radical trapping remains still an hypothesis.